We have studied 1st generation transplants of C3H/HeJ mammary tumors (FGMT) Lewis Lung Tumors (LLT) S-180 ascites (S-180A) tumor and Radiation Induced Fibrosarcoma (RIF) for responsiveness to corticosteroids in vivo. In these tumor models dexamethasone (Dex) methyl prednisilone (MP) and Triamcinolone Acetonide (TA) inhibit cell proliferation and tumor growth in a dose and agent dependent fashion. Dexamethasone is 3-4 times more effective in suppressing proliferation than is MP (RIF, FGMT, LLT). The steroid dose response curves for proliferation inhibition show saturation kinetics. MP and Dex apparently block cell cycle progression in G1, subsequently cells progress through S-phase after cessation of steroid treatment as indicated by changes in kinetic parameters. Sequential therapy with steroid plus 5-FU is schedule dependent with the best responses in terms of regrowth delay and increased survival noted when 5-FU was sequenced to coincide with maximal 3H-TdR LI during recovery from the steroid treatment. The levels of specific corticosteroid receptors in these models correlates with the antiproliferative effects of corticosteroids in vivo. Studies with other tumor models are underway to assess the relationship between receptor status and levels with responsiveness to corticosteroids in vivo.